Modification of Late Radiation Injury with L-Triiodothyronine

In 1895, Roentgen reported a new form of radiation. In 1896 Becquerel discovered radioactivity. In 1896 also the first cases of radiation dermatitis and epilation were observed (1). By 1902 radiation-induced cancer was reported (2). By 1910 the histopathology of late radiation changes had been documented (3). Each organ or tissue has been shown to have a characteristic pattern of structural and functional alterations which are produced as a late effect of exposure to ionizing radiation (4). These changes appear to be related to early injury to the vascular structures and to connective-tissue elements. This in itself may produce secondary changes in the parenchymal cell of the organ in question. In addition, the parenchymal cell may be injured directly by the ionizing radiation. The interplay of these two mechanisms, and doubtless others as yet unappreciated, results in altered structure and altered ability to perform a normal role in the economy of the body. These changes do not appear to reach a static state even at times far removed from the initial injury. It would appear, therefore, that the process is a dynamic one. Attempts to understand its mechanisms may lead to methods capable of perturbing the balance. Obviously, as clinicians we are interested in exploiting those methods which would result in a return to or toward normal. Attempts to alter the damage produced by ionizing radiation at the time it is initiated have included measures taken before and during irradiation. Attempts to modify established damage have for the most part been confined to a period of thirty days after exposure. With the exception of splenic and bone marrow transplants and their variants, no agent as yet has been found which, if given after irradiation, will modify radiation damage materially. The presence of such agents as cysteine, glutathione, cystamine, and AET at the time of irradiation appears to be necessary (5). There is some evidence that most of these protect against only one facet of the postirradiation syndrome, i.e., the causes of death from the ninth to the thirtieth day. Mice so protected may have a decreased life span. Renal pathology appears to be the most frequent cause of death in these initially protected animals (6). Attempts to alter established damage in patients have been sporadic and frustrating. Supportive measures such as transfusion for aplastic anemia or removal of severely damaged skin and underlying tissues followed by skin grafting are fairly routine. ACTH and cortisone were studied at one time because of their known suppressive effect on connective-tissue reaction to other injurious stimuli, with the hope that this effect might also be seen after irradiation. Unfortunately neither the animal experiments of Karnofsky (7) nor the human studies of Chu et al. (8) afforded any detectable evidence of beneficial effect.

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